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Questions and Answers
What is a common cause of chronic Candida vaginitis in individuals with diabetes?
Which factor is primarily responsible for the risk of nontraumatic lower extremity amputation in diabetes?
What condition can lead to the formation of maggots on wounds in diabetic patients?
Which of the following findings is indicative of diabetic retinopathy?
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What is a key sign of diabetic nephropathy?
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What psychological issue is commonly associated with type 2 diabetes?
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What is a dangerous behavior that young women with type 1 diabetes may engage in related to eating disorders?
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What is the primary goal of diabetes management regarding glycemic control?
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What is the primary characteristic of Type 1 Diabetes Mellitus (T1DM)?
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Which hormone is released when blood glucose levels are low?
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What complication is most commonly associated with Type 1 Diabetes Mellitus?
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Which of the following factors is NOT commonly associated with the etiology of Type 2 Diabetes Mellitus (T2DM)?
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What is the normal fasting blood glucose level range?
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What is a common result of glycogenolysis?
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Which condition is a result of severe hypoglycemia due to excessive insulin?
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What test assesses blood glucose levels over the preceding 3 months?
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Which syndrome is more associated with Type 2 Diabetes than Type 1?
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Why does hyperinsulinism lead to hypoglycemia?
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What condition results from the combination of insulin resistance and hyperglycemia in Type 2 Diabetes?
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Which of the following is a characteristic of diabetic nephropathy?
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Which classic sign of diabetes refers to increased thirst?
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What is the role of the hormone somatostatin in blood glucose regulation?
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Study Notes
Diabetes Mellitus (DM)
- Disorder of carbohydrate metabolism
- High blood glucose levels
- Body's inability to produce or utilize insulin
- Increased morbidity and mortality
- Increased risk of cardiovascular disease (CVD), renal damage, peripheral vascular disease, neurological disorders, blindness, and amputation
Four Major Categories of Diabetes Mellitus
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Type 1 Diabetes Mellitus (T1DM): Lack of insulin production due to destruction of beta cells in pancreas
- Insulin treatment required
-
Type 2 Diabetes Mellitus (T2DM): 90% of those with diabetes
- Insulin resistance present
-
Gestational Diabetes Mellitus (GDM): Develops during pregnancy
- Hormone changes reduce insulin sensitivity
- Increased risk of macrosomia (large baby)
- Other: Pancreatitis, cystic fibrosis, and neonatal diabetes
Epidemiology
- Over 30 million people in the United States
- Prevalence parallels obesity increase
- Sedentary lifestyle contributes
- Prevalence increases with age
- Polygenic disorder, a mutation in multiple genes
- Environmental factors play a role
Etiology
-
T1DM: Autoimmune destruction of beta cells
- Antibodies present
- Body does not produce insulin
-
T2DM: More gradual onset
- Insulin resistance
- Insulin still produced
- Sedentary behavior and obesity common factors
Insulin and Carbohydrate Ingestion
- Insulin is produced by beta cells and facilitates glucose movement from blood to cells
- Carbohydrate ingestion results in synchronous rise and fall of glucose and insulin
- As glucose elevates, insulin increases
Insulin Facilitates Glucose Uptake
- Insulin increases glucose uptake by cells
- Helps regulate blood glucose levels
Carbohydrate Metabolism Overview
- Glucose: Used for energy, stored as glycogen, and converted to components of lipid molecules
- Glycogenesis: Glycogen formation, primarily in liver and muscle
- Glycogenolysis: Glycogen breakdown when blood glucose levels are low
- Gluconeogenesis: Amino acids and glycerol of lipids converted to glucose in the liver and kidneys
Ketone Formation and Diabetic Ketoacidosis (DKA)
- DKA primarily affects Type 1 diabetes
- Ketone formation occurs when glucose cannot be utilized
- Ketones are strong acids that alter blood pH, leading to metabolic acidosis
Blood Glucose Levels
- Normal Blood Glucose: 70-100 mg/dL (fasting)
- Hypoglycemia: Blood glucose below 70 mg/dL
-
Impaired Glucose Tolerance (IGT): Prediabetes
- Fasting blood glucose 100-125 mg/dL
- Diabetes: Fasting blood glucose greater than 126 mg/dL
-
Postprandial Blood Glucose: Glucose after eating
- Greater than 200 mg/dL indicates diabetes
Role of Insulin
-
Muscle and Liver: Glycogenesis
- Insulin is an anabolic hormone
- Adipose: Reduces lipolysis
-
Hyperinsulinism: Increased insulin levels may occur to overcome insulin resistance
- This may require increased insulin administration
- Hypoglycemia: Too much insulin can cause low blood glucose levels
Other Glucose-Regulating Hormones
-
Glucagon: Released from alpha cells of pancreas when blood glucose levels are low
- Injectable form used in severe hypoglycemia
-
Somatostatin: Released from delta cells of pancreas
- Diminishes the secretion of insulin and glucagon
- Decreases gastrointestinal (GI) activity and slows absorption
-
Incretins: Released from GI tissues
- GLP-1 and GIP are GI glucose-regulating hormones that stimulate insulin and slow GI motility
-
Cortisol: Released from the adrenal cortex
- Increases blood glucose levels
Glucose-Regulating Signals From Pancreas
- The pancreas plays a critical role in blood glucose control
- Insulin and other hormones regulate glucose levels
T1DM: Pathological Mechanism
- Autoimmune disease caused by obesity and T cells attacking the body
- T cell mediated attack of beta cells
- Genetic influence
- DKA is often the presenting sign: Polyuria, polydipsia, and polyphagia
T2DM: Pathological Mechanism
- Insulin resistance with increased insulin levels
- Molecular-level mechanisms include oxidative stress, inflammation, insulin receptor mutation, and mitochondrial dysfunction
- Metabolic syndrome, characterized by hypertension, dyslipidemia, hyperinsulinism, and centralized obesity
- Hyperosmolar hyperglycemic syndrome (HHS) may occur but DKA is less common. Some insulin is still produced, preventing ketone formation
Gestational Diabetes Mellitus (GDM)
- Hormones of pregnancy increase insulin resistance
- Complications include fetal defects, premature delivery, newborn hypoglycemia, and macrosomia
- Screening involves a 2nd trimester oral glucose tolerance test (OGTT)
- GDM usually resolves after pregnancy but increases the risk of developing T2DM in the future
Diabetes Tests
- Blood Glucose: Fasting and random blood glucose levels
- Oral Glucose Tolerance Test (OGTT): 75g glucose ingested, blood glucose levels are measured
- Glycated Hemoglobin (A1c): Assesses blood glucose levels over the preceding 3 months
- Estimated Average Glucose (eAG): Average blood glucose over the last few months
- Islet Cell Autoantibodies (ICAs): Present in T1DM
-
C-peptide Test: Indicator of endogenous insulin
- C-peptide is released when the pancreas releases insulin
- Helps differentiate between T1DM and T2DM
Diabetes Tests: Urinalysis
-
Glucosuria: Elevated blood glucose leads to increased glucose filtration in the glomerulus
- Glucose appears in urine when renal glucose transport maximum is exceeded
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Ketonuria: Ketone formation and renal filtration of ketones are elevated
- More common in T1DM
Complications of DM
- Can be both acute and long-term
- Both hypoglycemia and hyperglycemia are possible
- Acute Complications: DKA (T1DM), HHS (T2DM)
- Long-Term Systemic Complications: Blindness, kidney failure, neuropathy, cardiovascular disease, and amputation
Hypoglycemia
- Blood glucose less than 70 mg/dL
- Causes: Excessive exogenous insulin, inadequate food intake, excessive physical activity, infections, illness, or drug interactions
- Compensatory response: Epinephrine, glucagon, and activation of the sympathetic nervous system (SNS) raise blood glucose levels
- Management: Fast-acting carbohydrates (15g), IV glucose, or subcutaneous injection of glucagon
Somogyi Effect and Dawn Phenomenon
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Somogyi Effect: Morning hyperglycemia due to hypoglycemia during sleep
- Excessive insulin therapy or insulin peak may be contributing factors
- Compensatory mechanisms raise blood glucose levels
-
Dawn Phenomenon: Morning hyperglycemia without hypoglycemia during sleep
- Nocturnal elevation in growth hormone may raise blood glucose levels
- Cells utilize less glucose at night
Classic Signs of Diabetes Mellitus
- Polydipsia: Increased thirst due to high blood glucose increasing plasma osmolarity and fluid shifts
- Polyphagia: Increased appetite due to cells not being able to utilize glucose effectively
- Polyuria: Increased thirst and drinking (polydipsia) lead to increased renal glucose filtration and osmotic diuresis (water follows glucose into the urine)
Fluid Shifts
- High blood glucose disrupts fluid balance
- Fluid shifts from intracellular fluid (ICF) to extracellular fluid (ECF)
Fluid and Glucose in Urine
- Increased glucose and water in urine
- Reflects kidney function and fluid removal
Additional Signs of DM
- Blurred Vision: Accumulation of glucose in the aqueous fluid of the eye changes light refraction
-
Fluid/Electrolyte Imbalance: Fluid shifts from ICF to ECF and electrolyte shifts
- Can lead to dilutional hyponatremia and potassium shifting out of cells
Diabetic Ketoacidosis (DKA)
- Insulin lacking: Cells use glucose for fuel, preventing lipolysis
- Without Insulin: Ketone formation occurs as cells cannot utilize glucose
- Ketones: Strong acids that lead to metabolic acidosis
- DKA is more common in T1DM: Some insulin is still produced in T2DM, preventing ketone formation
Diabetic Ketoacidosis (DKA): Diagnostic Criteria and Presentation
- Diagnostic Criteria: Blood glucose greater than 250 mg/dL, pH less than 7.3, bicarbonate less than 18 mEq/dL, blood osmolarity greater than 20 mOsm/L
- Presentation: Nausea, vomiting, and dehydration
Hyperosmolar Hyperglycemic Syndrome (HHS)
-
Hyperglycemia: Inability to facilitate glucose uptake
- Gluconeogenesis and glycogenolysis exacerbate hyperglycemia
- Hyperosmolarity: Elevated blood glucose leads to osmotic diuresis and polyuria
- Clinical Progression: Gradual development over days to weeks
- Patient Presentation: Weakness, poor tissue turgor, tachycardia, thready pulse, and confusion (25% of patients present in coma)
- Causes: Infection, trauma, and noncompliance with diabetes management
- Treatment: Fluids are administered first, followed by insulin to address plasma osmolarity issues
Long-Term Complications of DM
-
Arteriosclerosis: Damage to endothelial cells
- Leads to foam cells upon macrophages
- Peripheral Angiopathy: Lack of circulation
- Diabetic Retinopathy: Damaged eye vessels
-
Diabetic Neuropathy: Damaged kidneys
- Nephrocytes are damaged
- Autonomic Neuropathy:
- Diabetic Nephropathy:
- Poor Wound Healing: Decreased blood flow and high sugar levels create an environment where bacteria can grow easily, leading to slow healing
- Immunosuppression:
Long-Term Complications of DM: Factors and Effects
- Arteriosclerosis: Myocardial infarction (heart attack)
- Peripheral Angiopathy: Limb ischemia (lack of oxygen to blood vessels)
- Diabetic Retinopathy: Blindness
- Diabetic Neuropathy: Lack of sensation in lower extremities, burning, tingling
- Autonomic Neuropathy: Poor autonomic control
- Diabetic Nephropathy: Kidney failure
- Poor Wound Healing: Gangrene (necrotic tissue)
Long-Term Complications of DM: Risk Factors
- Duration of Chronic Hyperglycemia: - Damage to small and large arterial vessels - End-organ damage - Poor wound healing - Macrovascular damage
- Genetic Susceptibility:
DM and Atherosclerosis
- Acute Cardiac Events: 2-4 times more likely in diabetes patients
- Atherosclerosis: Affects large and small arteries
- Vascular Damage: Multiple processes contribute to damage, all linked to hyperglycemia and oxidative stress
DM and Peripheral Neuropathy
- Distal, Symmetric Polyneuropathy: Neural arteries are damaged, starting in the feet and progressing upwards
- Sensorimotor Nerves: Burning and tingling in the feet, blunted pain sensation
- Signs of Injury: Silent heart attack, motor weakness, gait abnormality, Charcot joint
DM and Autonomic Neuropathy
- Cardiac: Tachycardia, hypotension
- GI: Gastroparesis, gastric emptying abnormality, anorexia, nausea, bowel dysfunction
- Urinary: Increased risk of urinary tract infections (UTIs)
- Reproductive: Erectile dysfunction
- Temperature Regulation: Decreased sweating, hyperthermia, dry skin
- Glycemic Control: Hypoglycemia may be less noticeable due to altered signs and symptoms
DM and Susceptibility to Infection
- WBC Function: Reduced white blood cell function
-
Increased Colonization: Staph aureus and Candida (yeast)
- High glucose levels change vaginal pH allowing Candida to proliferate
DM and Amputation
-
Diabetic Foot Complications: Most common cause of nontraumatic lower extremity amputation
- Peripheral neuropathy, poor circulation, and suppressed immune response lead to increased infection susceptibility
- Can lead to gangrene and amputation
- Osteomyelitis (bone infection)
DM and Poor Wound Healing
- Reduced circulation and high sugar levels create environments that make it difficult for wounds to heal
DM and Foot Care
- Examine feet for sensation, including light touch
- Assess Achilles tendon reflex
- Check toe position
- Examine for injuries or wounds
DM and Retinopathy/Blindness
- Leading cause of blindness in adults
- Retinal Circulatory Damage: Microaneurysms, macular edema, and cotton wool spots (infarcted regions of retina)
- Proliferative Retinopathy: New vessel growth that is fragile and may rupture, leading to retinal detachment
- Regular Fundoscopic and Ophthalmological Exams: Critical to detect and manage retinopathy
DM and Nephropathy
-
Renal Failure: Damage to the glomerular capillaries
- Microalbuminuria (protein in the urine) may be present
- Glomerular Basement Membrane: Thickens due to glycosylation end-products
- Activation of RAAS: Worsens the problem by elevating blood pressure
DM and Dermatological Issues
- Prolonged Wound Healing and Ulcer Formations:
- Diabetic Skin Spots: Hyperpigmented areas
- Acanthosis Nigricans: Tiny, hyperpigmented, macular lesions
- Lipoatrophy: May occur at insulin injection sites
DM and Psychological Resistance
-
Depression: Twice as common in individuals with diabetes
- Guilt, discouragement, and self-blame are common, especially with type 2 diabetes
- Anxiety related to disease management
- Denial and noncompliance may occur
- Psychological Insulin Resistance: Refusal to comply with insulin management
DM and Eating Disorders
- Young Women with T1DM: At higher risk for eating disorders
- Insulin Purging: Restricting or skipping insulin usage to stimulate lipolysis and weight loss
- Suspect Eating Disorder: Patients with recurrent DKA or chronically poor glycemic control
DM Treatment Overview
- Blood Glucose Control: Managing both hyperglycemia and hypoglycemia
- Glycemic Control: Primary goal to reduce the risk of complications
- Reduce CVD Risk: Lipid panels, LDL below 60 mg/dL, and triglyceride management
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Description
Explore the major categories of Diabetes Mellitus, including Type 1, Type 2, and Gestational Diabetes. Understand the metabolic disorder's impact on health and its rising prevalence in the United States. Delve into the associated risks and the necessity of insulin treatment.
